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Disease and Defense > Unit 4a > Flashcards

Unit 4a Flashcards

1
Q

Peptidoglycan layer

A

rigid mesh, surrounds cytoplasmic membrane

Peptidoglycan → allows for maintenance of shape and resistance of osmotic pressure

Unique and required bacterial structure

Great target for many antibiotics

Recognized by host innate immune system

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2
Q

Structure of peptidoglycan layer

A

Polymer of repeating units of 2 hexose sugars, crosslinked

N-acetylglucosamine (GlcNAc)

N-acetylmuramic acid (MurNAc): linked to tetrapeptide chains with AA unique to bacterial cell walls

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3
Q

Capsules

A

gelatinous outer surface layer, coats surface of bacterial cells

Consist of complex polysaccharides

Function: Enhance virulence, resist phagocytosis

Antigenic (used in vaccines)
-Protein-capsular polysaccharide CONJUGATE vaccine may be required to vaccinate young children

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4
Q

Glycocalyx

A

form microbial biofilms (communities of bacteria)

“Slime layer” connects/embeds bacteria together/to surfaces

Protects cells from phagocytosis, host defenses (complement, antibody, defensins), limits access of abx to cells embedded in “slime layer”

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5
Q

Flagella

A

Originate in cytoplasmic membrane

Function in motility, bacterial chemotaxis

Peritrichous = flagella distributed over their surface
Polar = one/many flagella at one end

Move in a rotation: Run and Tumble based on direction of rotation

Antigenic (H antigens) - used in vaccines

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6
Q

Pili

A

long slender, proteinaceous antigenic, hair-like structure on surface of bacteria

Role in adherence to surfaces/tissues

Antibody can block adherence/confer resistance to infection

Sex pili → role in bacterial conjugation

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7
Q

Bacterial Secretion Systems

A

deliver proteins from cytoplasm of bacteria directly to target cell → alter cell function (alter actin cytoskeleton, host signaling, transcription)

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8
Q

Bacterial cytoplasmic membrane

A
  • physiological barrier between inside/outside of bacterial cell
  • Lipid bilayer (phospholipids, proteins (60-70%), NO sterols)

-Selective permeability
Only permeable to uncharged, hydrophobic molecules, smaller than glycerol

Contains electron transport system → generate proton motive force during respiration

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9
Q

Bacterial cytoplasm

A

aqueous solution, proteins + metabolites

-contains DNA (no nuclear membrane)

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10
Q

Bacterial ribosomes

A

70S, mRNA can be polycistronic

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11
Q

Bacterial nucleoid

A

DNA of bacteria located in this distinct region

DNA tightly packed, supercoiled

No nuclear membrane → transcription/translation coupled

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12
Q

Bacterial chromosome

A

single ds-circular DNA

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13
Q

Bacterial plasmid (4)

A

extrachromosomal, self-replicating, DNA molecules

Smaller than chromosomes

Not essential for viability

R Factors: genes that carry resistance to antibiotics

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14
Q

Bacteriophages

A

viruses that infect bacteria

Can integrate into bacterial chromosomes and replicate as part of the chromosome

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15
Q

Gram+ bacteria

A

Thick, extensively cross-linked peptidoglycan layer, also contains:

  • teichoic acids
  • Lipoteichoic acids
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16
Q

Techoic Acids

A

repeating polyglycerol-P or polyribitol-P backbone covalently attached to peptidoglycan layer

-embedded in peptidoglycan layer of gram + bacteria

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17
Q

Lipoteichoic acids

A

attached to underlying cytoplasmic membrane - anchors cell wall to membrane

present in gram+ bacteria

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18
Q

Function of teichoic acids (3)

A

1) Ion homeostasis
2) Adherence and colonization
3) Interacts with innate immune system through TLR for bacterial recognition and inflammation

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19
Q

Gram + stains ______, while gram - stains _______

A

purple

red

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20
Q

Bacterial endospores

A

Produced by some G+ bacteria (Clostridium, Bacillus)

Dormant (non-growing, non-metabolising) - resting stage to endure tough times - when environment improves it will grow

Highly resistant to environmental stresses, high temp, disinfectants, desiccation, oxygen

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21
Q

Gram- bacteria

A

Thin, sparsely cross-linked peptidoglycan layer with other major components on exterior of peptidoglycan

-Second outer membrane

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22
Q

What is contained in second outer membrane of gram-neg bacteria? (4)

A

asymmetric lipid bilayer

1) Lipopoilysaccharide
2) Lipoproteins
3) proins
4) phospholipids

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23
Q

Lipopolysaccharide (LPS) made up of ______, ______, and ______ located exclusively on the _______ of the second outer membrane.

LPS can be recognized by _________

A 
Lipid A (endotoxin)
Core polysaccharide
O side chain oligosaccharides (somatic antigens, O antigen)

outer leaflet

innate immune system –> inflammation and endotoxic shock

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24
Q

Bacterial growth

A

Growth via binary fission → two cells of equal size

All bacteria are thus the same “age”

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25
Q

4 phases of bacterial growth

A

1) Lag phase
2) Exponential phase
3) Stationary phase
4) Death phase

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26
Q

Lag phase

A

period of physiologic adjustment (inoculum)

Establish proper intracellular environment for optimal growth

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27
Q

Exponential phase

A

rate of cell division maximal for available nutritional conditions

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28
Q

Stationary phase

A

essential nutrients are consumed, toxic products of metabolism accumulate

Cell growth slows or ceases

Slow growing cells can be resistant to abx

Where bacteria spend most of their time in nature

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29
Q

Death phase

A

number of viable bacteria decrease over time

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30
Q

Heterotrophic vs. autotrophic bacteria

A

Heterotrophic bacteria: require organic carbon source

Autotrophic: obtain carbon exclusively from CO2

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31
Q

Fastidious bacteria

A

require, in addition to sources of carbon/energy, a number of essential growth factors

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32
Q

Obligate intracellular bacteria

A

growth within eukaryotic cells, cannot be cultivated on artificial media

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33
Q

Aerobic bacteria

A

require oxygen for growth

Produce ROS, and thus must produce catalase, superoxide dismutase, etc. to protect themselves against ROS

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34
Q

Anaerobic bacteria

A

do not require oxygen for growth

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35
Q

Indifferent bacteria

A

ferment in presence or absence of O2

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36
Q

Facultative bacteria

A

respire with O2, ferment in absence of O2

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37
Q

Sporulation

A

response to adverse nutritional condition

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38
Q

Spores

A

specialized cells produced by certain bacteria when nutritional supply is limited

Adapted for prolonged survival under adverse conditions
Can convert back to vegetative cells via germination

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39
Q

______ + _______ = “Energy Currency”

A

ATP + electrochemical gradient

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40
Q

Fermentation

A

catabolic, organic compounds are e- donors and acceptors

No net oxidation of substrates

Anaerobic, facultative/indifferent bacteria that grow under anaerobic conditions must get energy via fermentation of organic substrates
CANNOT do respiration

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41
Q

Respiration

A

generate ATP via e- transport, use O2 as final e- acceptor

Anaerobic respiration → use inorganic substrates as e- acceptor

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42
Q

Mechanisms of genetic variation (3)

A

1) Spontaneous Mutation
2) Recombination
3) Acquisition of new DNA segments

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43
Q

Spontaneous mutation

A

spontaneous single base change, deletion, insertion

Selective pressure for preferential growth of preexisting mutant within a population

→ resistance to antimicrobials, DOES NOT HAPPEN BERY OFTEN

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44
Q

Recombination

A

Site-specific or homologous recombination within a particular organism

OR genetic exchange/recombination between closely related organisms
→ new strains, new properties

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45
Q

Acquisition of new DNA segments

A

acquire new genes by LATERAL TRANSFER from other bacteria, or unrelated species
→ Alters virulence potential, survival characteristics, or antimicrobial resistance

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46
Q

Transposable elements

A

segment of DNA contained in bacteria/phage chromosome/plasmid that is enzymatically moved from one DNA location to another

(can make it mobile if it goes to a plasmid!)

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47
Q

How can you acquire new DNA segments? (4)

A

1) Transposable elements
2) Bacteriophage conversion
3) Acquisition of plasmids
4) Acquisition of pathogenicity islands

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48
Q

Conjugative plasmids

A

self-transmissible, mediate their own transfer between cells

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49
Q

Non-conjugative plasmids

A

mobilizable - can be passively transferred during conjugation

Can still be transferred by transformation or transduction

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50
Q

Bacterial plasmids can be transferred by _________ in gram+ bacteria

A

generalized transduction

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51
Q

Pathogenicity Islands

A

Insertions of one or more genes when comparing the genomes of two isolates of same species

-Encode genes that influence pathogenicity of strain

-Often appear as if acquired from an unrelated organism
(Genetic characteristics of bacterial viruses)

-Acquisition/loss important for evolution of pathogen

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52
Q

Transformation

A

Exchange of naked DNA of naked plasmid DNA (released from lysing cells)

DNA uptake into bacterial chromosome occurs only at certain points in growth cycle - specialized proteins needed to mediate uptake

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53
Q

Transduction

A

Gene transfer mediated by bacteriophage

Bacteriophage transfers segments of plasmid or chromosomal DNA from one cell to another

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54
Q

Conjugation

A

Genetic transfer dependent upon physical contact between donor and recipient cells - mediated by bacterial plasmids

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55
Q

Mechanisms of conjugation:

A

1) Cells come in contact, conjugation initiated (sex pilus bridges F+ and F- cell)
2) ss nick on oriT and binding of protein at 5’ end (in F+ cell) → initiate rolling circle replication
3) ss DNA transferred to F- cell via bridge and complementary strand synthesized
4) Cells separate at end of transfer

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56
Q

Conjugative transposons

A

DNA element that can excise themselves to form a covalently closed circular intermediate.

-circular intermediate can either reintegrate in the same cell (intracellular transposition) or transfer by conjugation to a recipient and integrate into the recipient’s genome (intercellular transposition)

Can encode abx resistance (esp Tetracycline)

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57
Q

Lytic state

A

Adhere to bacteria, inject DNA into bacteria

Progeny virus assembly/multiplication in cell and host cell lysis

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58
Q

Lysogenic state:

A

host cell remains viable, infecting phage DNA maintained by host cell in noninfectious state = prophage

Viral DNA injected, integrates into host chromosome → replicated as part of host chromosome (keep lytic stuff silent)

Maintained by prophage-encoded repressor protein that inhibits lytic development (can transform to lytic state)

Can convert phenotype of bacterial cell by formation of a lysogen

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59
Q

Prophage

A

phage DNA passively replicated as part of bacterial chromosome

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60
Q

Lysogenic Conversion

A

Temperate bacteriophages encode gene only expressed during lysogenic state → new phenotype in lysogenic host

Genes controlling the new phenotypic trait found ONLY as a component of the phage genome (not normal constituent of bacterial genome)

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61
Q

Generalized transduction

A

Any segment of donor cell genome may be passed into another cell

Sometimes get bacterial chromosomal DNA in virus capsule instead of viral DNA as an error during phage assembly

→ Integrate piece of bacterial DNA into another bacteria cell

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62
Q

Staphylococcus aureus is ______, _______ and ______ positive

A

catalase, coagulase, and gram

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63
Q

Staph. aureus abx resistance (3)

A

ABX resistance a serious concern

1) Penicillin-R
2) Methicillin-R (MRSA)
3) Vancomycin-R (emerging)

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64
Q

Manifestations of disease in staph aureus is…

A

STRAIN DEPENDENT

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65
Q

3 common types of diseases with staph aureus

A
  1. Cutaneous infection (localized focal abscess, can still spread)
  2. Toxinogenic infections (SSSS, TSS, food poisoning)
  3. Pneumonia (immunosup. with ~50% mortality)
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66
Q

staph aureus has ______, _______, ________ and _______ associated with its cutaneous infections

A

1) fibrin capsule
2) coagulase
3) alpha-toxin
4) foreign bodies

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67
Q

Coagulase and fibrin capsule of staph aureus act to…

A

wall off bacteria

68
Q

alpha toxin of staph aureus acts to…

A

Pore forming, damage tissue, interfere with phagocytosis/killing

69
Q

Toxinogenic Diseases of staph aureus (3)

A
  1. Staph Scalded Skin Syndrome (exfoliatins –epidermis falls off)
  2. Toxic Shock Syndrome (TSS) – Local infection, syst. toxic production of superantigen (T cell activation regardless of antigenic specificity)
  3. Food Poisoning from super-antigen contaminated food
70
Q

Where is staph aureus naturally located in the body

A

Anterior nares, Perineum,

Normal flora - may be source of infection

30% of people are asymptomatic carriers of staph aureus

71
Q

Staphylococcus epidermidis is ______ positive but ______ negaive

A

gram

coagulase

72
Q

abx resistance and difficulties with treating staph epidermidis

A

Makes BIOFILMS on devices hard to treat
-often device must be removed

Abx resistance:
1) Methicillin-R

73
Q

Typical staph epidermidis infections

A

Localized infections associated with foreign bodies (catheters, shunts, artificial/ damaged heart valves, hip prostheses)

74
Q

Staph epidermidis generates ________ which makes it hard to treat

A

Glycocalyx (gooey ploysac.) producers (allow organisms to adhere tenaciously to various implanted devices and grow in biofilm on device surface)

75
Q

Infection with staph epidermidis

A

Normal skin flora
-fairly non-pathogenic, but may be associated with localized infections

Nosocomial infections

Normal flora enters on foreign body

76
Q

Microbial toxins

A

macromolecular products of microbes which cause harm to susceptible animals by altering cellular structure or function

Can cause major manifestations of specific diseases

Can contribute to pathogenesis without causing unique signs or symptoms

Toxin-mediated diseases cause significant morbidity and mortality

77
Q

Toxins that facilitate spread of microbes through tissues act by…

Examples

A

breaking down ECM, degrading debris

EX) hyaluronidase, collagenase, elastase, phospholipase, streptokinase, deoxyribonuclease produced/secreted by bacteria

78
Q

Toxins that damage cellular membranes include ______ and ______ and act by….

A

hemolysins, cytolysins

Can kill target cell, form pore in membrane or degrade membrane → lyse cells

79
Q

Hemolysins

made by ______ and _______

mechanism of action

A

(lyse RBCs) - many varieties

EX) Staph aureus, strep pneumoniae

Insert into membrane and form pore = pore forming toxins

80
Q

Cytolysins

A

lyse RBCs and other cells too

81
Q

Superantigens

A

most potent T cell activators, aberrant activation of T cells

Bind MHC class II on APCs and to specific V chains on T cells (at site different from antigen-binding site) → activate LARGE number of T cells

Stimulate excessive production of cytokines

82
Q

______ and ______ make 19 different types of superantigens and can cause diseases such as _______, _______, and _______

A 
Staph aureus (TSST)
Strep pyogenes (pyrogenic exotoxins)

Toxic Shock Syndrome, food poisoning, necrotising fasciitis

83
Q

________, ________, _______, _______ and ________ inhibits protein synthesis irreversibly

A 
Diptheria toxin
Pseudomonas aeruginosa
Shiga toxins
Ecoli toxin
Ricin
84
Q

Diptheria toxin

A
  • Inhibits protein synthesis by modifying EF-2 in euk cells
  • Toxin made locally and disseminates throughout whole body
  • Specific receptors on target organisms - doesn’t affect cells that lack the specific receptor

1 molecule of diphtheria can kill 1 eukaryotic cell

If you have antitoxin you are protected against diphtheria → need immunization + boosters

85
Q

Pseudomonas aeruginosa toxin

A

produces toxin with same mechanism as diptheria (EF-2 modifiation)
–> BUT still require different toxoid immunization

Targets different organs than diphtheria (different receptor targets)

86
Q

Shiga toxins, Ecoli toxin, and Ricin

A

Act on ribosomal subunit to stop protein synthesis

-RNA N-glycosidases that remove residue from 60S subunit –> inactivate ribosomes

All have different effects based on receptors they target

87
Q

Vibrio Cholerae toxin

A
  • cell signal pathway modification
  • increases cAMP –> active Cl- secretion –> secretory diarrhea and massive water loss

-targets small intestine

88
Q

Pertussis toxin

A

Modify intracellular signaling pathways

Increases Adenyl cyclase activity-> increase cAMP

89
Q

Anthrax edema factor (EF) and Anthrax lethal factor (LF)

A

Toxins that modify intracellular signaling pathways

Edema factor → increase AC activity –> increase cAMP –> water influx

Lethal factor → breaks down signaling proteins (kinases)

90
Q

Toxins that inhibit release of neurotransmitters (2)

A

Botulinum toxin, tetanus toxin

Same activity inside cell, but different target cell causes different manifestations of toxin

  • Zinc dependent endopeptidases
  • inactivate SNARE proteins required for exocytosis
91
Q

Botulinum toxin

A

anaerobic → can be ingested with home canning

Flaccid paralysis (inhibits release of ACh at myoneuroal junctions)

92
Q

Tetanus toxin

A

anaerobic → requires deep wound that is anaerobic

Rigid paralysis inhibits (inhibit NT release from inhibitory interneurons in spinal column)

93
Q

Bacterial protein toxins

aka ?
3 characteristics

A

aka EXOtoxins

Heat-labile, immunogenic, neutralized by abs

94
Q

Lipopolysaccharides (LPS)

aka ?

A

ENDO toxin

Part of outer cell membrane of gram-negative organisms

Can also be released and bleb off into the bloodstream

PAMP recognized by innate immune system, elicits host response

Low dose of LPS → activates macrophages, B cells, complement

High dose of LPS → DIC

95
Q

Toxins with intracellular targets

A

must cross plasma membrane

Bi-functional proteins: separate domains designated A (active) and B (binding)

Susceptibility or resistance to toxins determined by presence/absence of receptors on target cell

Use normal membrane constituents as receptors

Enter target cells by endocytosis

Active portion of toxin translocated to cytosol to interact with target

96
Q

Toxoid

A

immunogenic but NOT toxic

Used as vaccines for protection against toxin-mediated diseases

97
Q

Passive immunization

A

abs given to patient for temporary protection against toxin or infectious agent - neutralize specific toxin extracellularly (before toxin enters the cell)

Limited duration of immunity (abs degraded)

98
Q

Active immunization

A

give toxoid to elicit production of specific anti-toxic abs

Primary series + periodic booster doses to maintain protection

Active immunity persists for many years due to immunologic memory

99
Q

Immunotoxins

A

hybrid molecules, toxin fragment (without receptor binding domain) linked to ligand, ab or hormone that binds specific receptor (different receptor from native toxin)

Enable immunotoxin or hormonotoxin to bind cells that express the alternative receptor and intoxicate them

Designed to kill tumor cells with tumor-specific receptor, but not kill normal cells without receptor

100
Q

Antitoxins

A

bind to toxins and prevent their toxicity (neutralization)

DO NOT prevent infection by toxin producing bacteria, or reverse effects after toxin has entered host cells

101
Q

Streptococcus pyogenes is also known as ________.

It is Gram _____ _______

A

Group A strep (B-hemolytic)

Gram + cocci

102
Q

Types of infections seen with strep pyogenes infection (5)

A

1) Glomerulonephritis (due to cross reactive ab)
2) Rheumatic fever (cross-reactive ab)
3) Infective endocarditis
4) Skin/wound infections (cellulitis)
5) Strep throat

103
Q

Infective endocarditis associated with strep pyogenes differs from rheumatic fever in that…

A

bacterial infection of the heart valves themselves - not due to cross-reactive ab

104
Q

M protein

2 main functions

A

primary virulence factor of strep pyogenes

-surface exposed protein

→ inhibits phagocytosis / killing by PMNs
→ enhances adherence to epithelial cells

105
Q

Why are there repeated infections associated with strep pyogenes? What is associated with recovery?

A

> 70 serotypes based on antigenic dif. in M protein → repeated infection

-M protein specific ab makes bacterial cell susceptible to killing, associated with recovery and immunity (to all antigenically related strains)

106
Q

Strep pyogenes is a normal flora bacteria present where?

A

the pharynx

107
Q

How is strep pyogenes spread?

A
  • Nasal secretions

- Droplets produced by coughing

108
Q

Streptococcus pneumoniae is a gram ______ ______

aka __________

A

gram + cocci

pneumococcus

109
Q

Types of infections associated with strep pneumoniae (invasive vs. non-invasive)

A

Noninvasive:

  • Pneumonia (~60% of bacterial pneumonia)
  • Sinusitis
  • Otitis media
  • Bronchitis

Invasive:

  • Meningitis
  • Bacteremia
110
Q

Strep pneumoniae has a __________ which allows it to grow and evade host defenses. Ab to this is associated with…

A

antiphagocytic polysaccharide capsule

(>91 different serotypes)

Recovery/immunity due to anti-capsular ab

111
Q

Why are the very young more susceptible to strep pneumoniae infection?

A

Very young more susceptible because less able to make ab to polysac capsule

-must give vaccine with conjugate polysaccharide

112
Q

Strep pneumoniae is a bacteria that is part of our normal flora where?

A

Upper respiratory tract

113
Q

People most susceptible to strep pneumoniae?

A

very young or old

alcoholism (mucocillary defect)

respiratory viral infection

114
Q

Enterococcus faecalis is a gram ______ _______

A

gram + cocci

115
Q

Enterococcus facecalis abx resistance

A

Intrinsic and emerging acquired abx resistance (Vancomycin-R)

116
Q

Common infection sites of enterococcus faecalis (3)

A

1) *Urinary tract (travels from GI → across perineum → up urethra = infection)
2) Surgical wounds
3) Biliary tract

117
Q

Transmission of enterococcus faecalis

A

Pt to pt on hands of healthcare workers or medical devices

118
Q

Enterococcus faecalis is a normal flora present in __________, and thus frequently casues _________

A

GI tract

Frequently cause of nosocomial infections

119
Q

Clostridium difficile is a gram _____ _____.

A

gram + rod

120
Q

Two MOST important characteristics of Clostrium bacteria

A

STRICT ANAEROBES

endospore formers

121
Q

Clostridium difficile abx resistance

A

Resistant to most abx

-spores resistant to hand sanitizer

122
Q

Manifestation of clostridium difficile infection

A

Diarrhea/pseudomembranous colitis following abx tx for unrelated conditions (esp. Clindamycin)

**disease due to depletion of intestinal flora = C. difficle overgrowth

123
Q

Virulence factor of Clostridium difficile

A

Two discrete toxins that damage intestinal mucosa = responsible for observed pathology and symptoms [enterotoxin + cytotoxin]

124
Q

Clostridium difficile is a normal flora present in the _______. It is thus responsible for many __________

A

GI tract

Nosocomial hospital acquired infection
-Usually from pt’s own gut flora

125
Q

C. Diff is associated with __________ in the hospital and is treated with ________

A

antibiotic associated diarrhea

TX: stop abx use, vancomycin or **metronidazole

126
Q

Clostridium tetani

A
  • Spores present in soil and animals

- Local infection must be anaerobic → toxic production

127
Q

Manifestation of clostridium tetani and mechanism of action

A

Retrograde transport of toxin to CNS

Block INHIBITORY INTERNEURONS in CNS

Prevents you from relaxing musculature
→ Spastic paralysis

128
Q

Vaccine and antitoxin for tetanus

A

Vaccine for tetanus (inactivated toxin)
Natural immunity does NOT occur - dose for immunization is more than dose that will kill you

Antitoxin - can be given after tetanus exposure

129
Q

Clostridium botulinum

A

Spores in soil and animals, can contaminate canned food

Botulinum is heat resistant (not killed with canning)

130
Q

Manifestation of clostridium botulinum and mechanism of action

A

Toxin blocks ACh transmission at neuromuscular junction→ flaccid paralysis, respiratory failure

Unable to innervate the musculature

131
Q

Staph aureus vs. clostridium perfringens food poisoning

A

Staph - from super-antigen contaminated food (pre-made toxin ingested) –> fast onset food poisoning

Clostridium perfringens - ingest microbe which then produces toxin (toxin made in vivo) –> slow onset food poisoning

132
Q

Clostridium perfringens manifestations of infection (2)

A

1) wound infections
2) food poisoning

strict anaerobe, makes spores

133
Q

Alpha toxin

A

phospholipase that kills phagocytic cells and muscle tissue

  • produced by Clostridium perfringens
  • responsible for wound infections
134
Q

Mechanism of action of food poisoning associated with Clostridium perfringens

A

Enterotoxin - exotoxin that acts on the gut

Ingest organisms from contaminated food

Toxin produced in vivo

Site of action is small intestine

135
Q

Mycoplasma Pneumoniae is special because…

A

it has no cell wall!

–> NOT susceptible to penicillins, vancomycin

136
Q

Type of infection associated with Mycoplasma Pneumoniae

A

Atypical pneumonia:

  • More common in younger persons (5-20 yrs)
  • Easily transmitted from person-person by respiratory secretions
  • Occurs in any season
  • Long period of shedding and very low infectious dose
  • Mild disease (“walking pneumonia”)
  • Non-productive cough
137
Q

Mechanism of action of Mycoplasma pneumoniae

A

Adheres to respiratory epithelial cells

Bacterial growth is extracellular

Produces H2O2 and superoxide radicals → damage host tissue

138
Q

Escherichia coli is a gram ______ ______

A

gram - rod

139
Q

E. Coli abx resistance?

A

Common resistance via acquisition of drug-resistant plasmid

140
Q

E. Coli is normal flora where?

A

the large intestine

141
Q

Types of infections associated with E. Coli (3)

A

GI disease
UTI
Abdominal infections

-Many different strains with varying pathogenic potential

142
Q

Mechanism of GI infection of E. coli (2 essential properties)

A
  1. Adherence to intestinal mucosa (pili)

2. Toxins that disrupt the electrolyte balance in the gut (GI disease)

143
Q

Mechanism of UTI infection of E. coli (3)

A
  1. Adherence to bladder epithelium
  2. Specific interactions with bladder epithelial cells
  3. Hemolytic = which are uncommon in the bulk of the intestinal population
144
Q

How do you acquire an E. coli GI infection?

A

drinking contaminated water or eating contaminated food

145
Q

How do you acquire an E. coli UTI infection?

A

endogenous flora from GI tract gets into urethra → bladder → kidney = access to UT

-special strains getting into the wrong place

146
Q

How do you acquire an E. coli infection in the abdomen?

A

Release/escape contents of colon to peritoneal cavity and adjacent tissues

-typically mixed infections with anaerobic bacteria –> anaerobic abdominal abscess

147
Q

ETEC (Enterotoxigenic E. Coli)

A
  • self-limiting
  • may require fluid replacement
  • GI infection
148
Q

Psuedomonas aeruginosa is a gram _____ _____

A

gram - rod

149
Q

Psuedomonas aeruginosa abx resistance?

A

Intrinsic resistance of P. aeruginosa to many abx

-difficulties delivering drug to site of bacterial replication

150
Q

Typical infections associated with pseudomonas aeruginosa (3)

A
  1. Infection of traumatic injuries, surgical wounds, and especially BURNS
  2. Chronic lung infection of CF pts.
  3. Hospital acquired infections (UTI, pneumonia)
151
Q

Psuedomonas aeruginosa is a common bacteria where?

A

the environment

-most people are highly resistant to infection by PA

152
Q

P. aeruginosa and CF

A
  • CF pts make copious, viscous bronchial secretions → stasis in lungs, predisposes pt to infection.
  • Early in life, pulmonary infections with S. aureus are relatively common, but are usually control with antimicrobials.
  • CF pts become chronically infected with P. aeruginosa by 15-20
  • aided by intrinsic resistance to many anti-staph drugs
  • Chronic lung infection with P. aeruginosa often cause of death in CF pts.
153
Q

P. aeruginosa bacteria are bad in CF patients because they are protected from phagocytes in the lungs by… (3)

This all leads to…

A

1) viscous lung secretions
2) mucoid exopolysaccharide made by bacteria
3) bacterial toxins

→ progressive damage to lungs due to toxins and host immune response

154
Q

Neisseria gonorrhoeae is a gram _____ ______

A

gram - diplococci

155
Q

Neisseria gonorrhoeae acquires antigenic variation via what?

A

Antigenic variation – change in pilus

-randomly modifies a.a. sequence of pilus protein = dramatic change in antigenic site

156
Q

Common infections associated with Neisseria gonorrhoeae (5)

A

1) Gonorrhea
2) Conjuctivits: leads to blindness in infants born to infected mothers (TX with abx at time of birth to prevent)

3) Urethritis
4) Fibrosis
5) Infertility

157
Q

Neisseria gonorrhoeae uses a _______ for ___________ and _______ as a key requirement for its virulence

A

pilus

adherence, and to avoid killing by neutrophils

-ab against pilus protective for that strain

158
Q

Neisseria gonorrhoeae in males vs. females

A

Males = asymp. to urethritis

Female = infection of cervix and urethra, ascending infection including uterine tubes = fibrosis and infertility

159
Q

Bacteroides fragilis is a gram _______ _______ that is ________

A

gram - anaerobic rod

aerotolerant

160
Q

Typical infections associated with bacteroides fragilis

A

anaerobic abscess below the diaphragm

161
Q

3 virulence factors of bacteroides fragilis

A

1) Tissue-destructive enzymes
2) Capsule (protects from phagocytosis)
3) Superoxide dismutase (protects an organism from the lethal effects of oxygen)

162
Q

Bacteroides fragilis is a normal flora where?

A

colon (in small numbers only)

163
Q

Chlamydia trachomatis is a ____________

A

obligate intracellular bacterium

164
Q

Infections associated with Chlamydia trachomatis (3)

A

Trachoma → chronic infection of conjunctiva → blindness

Genital infections (STD)

Neonatal infections → conjuctivitis and pneumonia

165
Q

Chalmydia trachomatis grows __________ and infects via ________

A

grows in vacule within host cell and infects via elementary bodies

166
Q

Chalmydia trachomatis infection in males vs. females

A
  • Males → urethritis
  • Females → urethritis, cervicitis, PID

associated with gonorrhea infections

Disease and Defense (11 decks)

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